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PubMedDate not supplied

[The effect of pharmacological preparations on the regulation of growth hormone secretion].

The authors have assessed the effects of 7 metabolic and 5 neutral drugs and their combinations on the basal blood concentration of the growth hormone (GH) and on the sensitivity of GH-regulating centers to homeostatic glucose inhibition. No significant changes in GH basal level were revealed. Nacom and a combination of vitamins E and C reduced the threshold sensitivity to glucose inhibition of the GH, whereas miscleron and trental elevated this threshold sensitivity. A combination of butamid and nacom had the highest stimulatory effect on the cellular immunity and macrophagal function, that may be mediated by enhanced GH secretion. In subjects with the 'superior' (android) type of obesity GH basal concentration and its sensitivity to glucose inhibition were lower than in those with the 'inferior' (gynoid) type, this being true after the drug discontinuation.

Breast Neoplasms↗
PubMed1976

A study of protein clearances in patients with nephrotic syndrome.

In 37 patients of nephrotic syndrome, serum protein levels, protein fractions and urinary levels of proteins and their fractions were determined. The findings of serum levels of proteins and their fractions were compared with an equal number of age and sex matched controls. Twenty three patients showed selective and 14 non-selective proteinuria. Most of the patients with selective proteinuria showed good response to steroids therapy while those with non-selective proteinuria did not respond.

Adolescent↗
PubMed1977

[Antibodies to thyroglobulin in patients with cancer].

Investigations of over 300 oncological patients and 120 healthy individuals have evidenced a considerable increase in the frequency of detecting antibodies to thyreoglobulin (in the titre 1/80 and higher) in patients with cancer of the breast, sigmoid and stomach in females and a tendency to such increase in cancer of the uterine body, and a number of other localizations.

Adult↗
PubMed1977

[Phenformin elimination of the immunodepression caused by 1,2-dimethylhydrazine in rats].

Treatment of rats with 1,2-dimethylhydrazine (SDMH) with the doze of 21 mg/kg per body weight once a week during four weeks caused the decrease of biogenic amine level, particularly, of dopamine in the hypothalamus, the decrease of glucose tolerance, the increase of the blood level of insulin and triglycerides. According to the previously achieved data SDMH causes the elevation of the hypothalamic threshold of sensitivity to the inhibitory action of estrogens. At the same time SDMH provides considerable suppression of lymphocyte blastogenic response to phytohemagglutinin and lipopolisaccharide, the decrease of the level of antibody produced against sheep erythrocytes, and the decrease of phagocytic activity of macrophages. Thus SDMH provides the syndrome of intensified aging. Recently our laboratory achieved the data, that antidiabetic drug-phenformin-improves cell-mediated immunity indices and the activity of phagocytosis in middle-aged subjects, as well as in patients with atherosclerosis and cancer (Vopr. Oncol., 1976, N 2, p. 13). On the basis of these findings phenformin (2 mg/day per os) was administered in rats in combination with SDMH. This resulted in restoration of all the abovementioned immunologic indices. It may be suggested that SDMH causes metabolic immunodepression, similar to the immunodepression, inherent to normal aging, pregnancy, stress and specific age-associated pathology--diseases of compensation (Vopr. Oncol., 1976, N 8, p. 3). If immunodepression is one of the components of cancerogenesis, then the elimination of metabolic immunodepression, which arises in course of normal aging or under the influence of cehmical cancerogens, can provide an anticancerogenic prophylactic effect.

Administration, Oral↗
PubMed1996

Alterations in brain tumor DNA detected by a fingerprinting probe.

We used a novel DNA fingerprinting probe O-chi-1 (ref. 1) to detect differences in the hybridization pattern of brain tumor DNA and paired normal tissue of a given individual. Representatives of meningiomas (two), glioblastoma multeforme (three) and astrocytoma (one) were studied. Alterations, which included amplification as well as the loss of a normal band in tumor DNA, were observed in four of the six tumours. While the increased intensity of a band can be taken to imply increased copy number, the disappearance of bands could either be due to loss of DNA sequence or rearrangement resulting in different sized bands.

Astrocytoma↗
PubMed1976

[Mutational-metabolic model of carcinogenesis and the progression of the neoplastic process].

The given data indicate the presence of a negative correlation between metabolic indices (a decrease of the tolerance to glucose, increase of the blood level of free fatty acids, insulin, cholesterol triglycerides, cortisol, stc) and the indices of cellular immunity, which is determined by the number of rosette-forming cells and blasttransformation reaction to PHA and skin tests. Accordingly, the administration of an antidiabetic drug-phenformin (phenetylbiguanide)--apart from the improvement of metabolic pattern, results in the restoration of the cell-mediated immunity indices. These findings provide a basis for stating the phenomenon of metabolic immunodepression. The metabolic immunodepression may be supposed to prevent immunological surveillance activation, which normally is realized through the signals, provided by cells subjected to somatic mutation. It is noteworthy that the given metabolic conditions (hypercholesterinemia, hyperinsulinemia, the enhanced utilization of free fatty acids) promote the division of somatic cells. Thus, the same metabolic shifts which increase the pull of proliferating cells and, accordingly, increase the possibility of mutation development, also cause the metabolic immunodepression at the same time. These opposite metabolic influences on somatic cells and T-dependent lymphocytes cause the development of the syndrome of cancrophilia. The syndrome of cancrophilia normally arises at pregnancy, in intensive growth of the organism in childhood, accelerated development, stress and during normal ageing. Many carcinogens cause the decrease of tolerance to glucose, the increase in blood-insulin level and elevation of the threshold of sensitivity of the hypothalamus to feedback suppression. This phenomenon is based on the decrease of catecholamine level in thehypothalamus in ageing, stress and the action of some carcinogens. Thus, the syndrome of cacrophilia provides the conditions for cancer development and tumor progression, besides, the tumor itself produces the metabolic shifts typical of cancrophilia. In the light of mutation-metabolic model of cancer development, it is possible to consider the fundamental factors which increase of hinder carcinogenesis.

Aging↗